1. Field of the Invention
The present invention relates to implantable medical devices and methods, and more particularly, to a dual-chamber implantable pacemaker or pacemaker system having enhanced upper rate behavior adapted to maintain a more appropriate ventricular frequency and to minimize the risk of a pacemaker-mediated tachycardia (PMT).
The basic function of the heart is to pump (circulate) blood throughout the body. The blood serves as a medium for delivering oxygen and nutrients to the various tissues while removing waste products and carbon dioxide. The heart is divided into four chambers comprised of two atria and two ventricles. The atria are the collecting chambers holding the blood which returns to the heart until the ventricles are ready to receive this blood. The ventricles are the primary pumping chambers. The pumping function of the heart is achieved by a coordinated contraction of the muscular walls of the atria and the ventricles.
The atria are more than simple collecting chambers. The atria contain the heart's own (natural, native or intrinsic) pacemaker that controls the rate at which the heart beats or contracts. In addition, the atrial contraction helps to fill the ventricle, further contributing to optimal filling and thus maximizing the amount of blood which the heart is able to pump with each contraction. Thus, atrial contraction is followed after a short period of time (normally 120 to 200 ms) by ventricular contraction.
The period of cardiac contraction during which the heart actively ejects the blood into the arterial blood vessels is called systole. The period of cardiac relaxation during which the chambers are being filled with blood is called diastole. Atrial and ventricular systole are sequenced allowing the atrial contraction to help optimally fill the ventricle. This is termed AV synchrony.
A cardiac cycle comprises one sequence of systole and diastole. It can be detected by counting the patient's pulse rate. It is also reflected by the cardiac rhythm as recorded by an electrocardiogram (ECG) or electrogram (EGM). The ECG is a recording of the electrical activity of the heart as seen using surface electrodes placed on the surface of the body. The EGM is a recording of the electrical activity of the heart as seen using electrodes placed within the heart. The electrical activity refers to the cardiac depolarization in either the atrium and/or ventricle. In general, on the ECG or EGM, the atrial depolarization is represented by a P-wave, while the ventricular depolarization is represented by a QRS complex, sometimes abbreviated as an "R-wave." The electrical depolarization triggers or initiates the active muscular contraction. Once the cardiac cells are depolarized, they must repolarize in order for the next depolarization and contraction to occur. Ventricular repolarization is represented by the T-wave. Atrial repolarization is rarely seen on an ECG or EGM as it occurs at virtually the same time as the R-wave, and is thus hidden by this large electrical signal.
A normal heart rate varies between 60 to 100 (bpm) with an average of 72 bpm resulting in approximately 100,000 heart beats per day. The heart beat normally increases during periods of stress (physical or emotional) and slows during periods of rest (sleep).
The amount of blood that the heart pumps in one minute is called the cardiac output. It is calculated by the amount of blood ejected with each heart beat (stroke volume) multiplied by the number of heart beats in a minute. If the heart rate is too slow to meet the physiologic requirements of the body, the cardiac output will not be sufficient to meet the metabolic demands of the body. Too slow of a heart rate, termed a bradycardia, may thus result in one of two major symptoms: (1) if the heart effectively stops with no heart beat, there will be no blood flow and if this is sustained for a critical period of time (10 to 30 seconds), the individual will faint; or (2) if there is a heart beat but it is too slow, the patient will be tired and weak (termed low cardiac output).
A pacemaker is a medical device that is used to selectively stimulate the heart with electrical stimulation pulses aimed at assisting it to perform its function as a pump. Normally, the stimulation pulses are timed to keep the heart rate above a prescribed limit, i.e., to treat a bradycardia. A pacemaker may thus be considered as a pacing system. The pacing system is comprised of two major components. One component is a pulse generator which generates the stimulation pulse and includes the electronic circuitry and the power cell or battery. The other is the lead or leads which electrically couple the pacemaker to the heart.
The pacemaker delivers an electrical stimulus to the heart to cause the heart to contract when the patient's own intrinsic rhythm fails. To this end, pacemakers include sensing circuits that sense the EGM, and in particular that sense the P-waves and/or R-waves in the EGM. By monitoring such P-waves and/or R-waves, the pacemaker circuits are able to determine the intrinsic rhythm of the heart and provide stimulation pulses that force atrial and/or ventricular depolarization at appropriate times in the cardiac cycle so as to help stabilize the electrical rhythm of the heart.
Pacemakers are described as either single-chamber or dual-chamber systems. A single-chamber system stimulates and senses the same chamber of the heart (atria or ventricle). A dual-chamber system stimulates and/or senses in both chambers of the heart (atria and ventricle). Dual-chamber systems may typically be programmed to operate in either a dual-chamber mode or a single-chamber mode.
A three letter code (sometimes expanded to a five letter code) is used to describe the basic mode in which the pacemaker is operating. These three letters refer specifically to electrical stimulation for the treatment of bradycardia. A fourth position (when used) identifies the degree of programmability and rate modulation, and a fifth position (when used) refers to electrical stimulation therapy for the primary treatment of fast heart rhythms or tachyarrhythmias or tachycardias.
The first position of the pacemaker code identifies the chamber to which the electrical stimulus is delivered. If the device is not capable of bradycardia support pacing, a "0" occupies this first position. If the unit paces in the ventricle, this is identified by a "V"; if it paces in the atrium, the first position is identified as an "A." If stimuli can be delivered to either the atrium or ventricle, the letter "D" is used to reflect dual-chamber stimulation.
The second position of the pacemaker code identifies the chamber or chambers in which sensing occurs. Sensing is the ability of the pacemaker to recognize the intrinsic electrical activity of the heart. The letters used in this position are identical to those used in the first position.
The third position of the pacemaker code identifies the way the pacemaker responds to a sensed signal. An "I" means that the pacemaker will be inhibited. When it senses or sees an intrinsic electrical signal, it inhibits its own output pulse and resets one or more internal timers within the pacemaker's circuitry. The other basic response is represented by a "T," which means triggered. The triggered mode of response indicates that when the pacemaker senses an intrinsic electrical signal, it not only resets various internal timers within the pacemaker, it also initiates or releases a stimulus in response to that sensed event. A "D" in the third position refers to both modes of sensing response. Most commonly, a sensed signal arising from the atrium and sensed on the atrial channel of a dual-chamber pacemaker will inhibit the atrial output but trigger a ventricular output after a brief delay (the AV delay). If a native ventricular depolarization does not occur before the AV delay timer completes, a ventricular stimulus will be released at the end of this AV delay. If a native ventricular signal is sensed within the AV delay, the ventricular output will be inhibited and other timers will be reset. If a native ventricular signal is sensed before the atrial stimulus is released, both the atrial and ventricular output pulses will be inhibited and the various timers will be reset.
A popular mode of operation for dual-chamber pacemakers is the DDD mode. DDD systems were developed to overcome the limitations of previous pacing methods. Specifically, DDD systems provide atrial pacing during atrial bradycardia, ventricular pacing during ventricular bradycardia, and atrial and ventricular pacing during combined atrial and ventricular bradycardia. In addition, DDD systems provide an atrial synchronous mode. Such features more closely approximate the normal response to exercise, or other physiological activity demanding a faster heart rate, by permitting a rate increase to occur commensurate with the rate of the sensed P-wave. This advantageously increases cardiac output and facilitates maintenance of AV synchrony.
Unfortunately, a pacemaker operating in the DDD mode may contribute, in combination with other factors, to a pacemaker-mediated tachycardia (PMT). For example, in patients who are prone to atrial arrhythmias, e.g., a fast atrial rate, the DDD pacer tracks the fast atrial rate, causing the ventricles to be paced at a correspondingly fast rate, thereby causing a tachycardia (fast heart rate) to occur. Without the DDD pacemaker, such tachycardia would probably not occur because the ventricles would normally continue at a slower (more normal) rate, despite the fast atrial rate. However, with the DDD pacemaker, the stimulation of the ventricles occurs so as to track the fast atrial rate, and thus the pacemaker effectively intervenes or "mediates" so as to cause the tachycardia, appropriately termed a "pacemaker-mediated tachycardia," or PMT, to occur.
There are also other reasons why a PMT may be triggered by a DDD pacer, other than simply tracking a fast atrial rate. For example, prolonged intervals between atrial and ventricular depolarization can cause or enhance retrograde conduction of P-waves, which retrograde P-waves are sensed by the pacemaker sensing circuits. Unfortunately, the pacemaker sensing circuits cannot differentiate between retrograde P-waves or normal P-waves, so such sensing may result in a PMT wherein each ventricular paced event is followed by a retrograde P-wave which is tracked, resulting in another ventricular paced event, causing the process to repeat.
It is well known that the type of PMT described above (resulting from sensing retrograde P-waves) can be prevented by programming the post ventricular atrial refractory period (PVARP) of the pacemaker to be longer than the retrograde conduction time. Such lengthening of the PVARP, however, disadvantageously prevents the sensing of a P-wave that occurs late in the PVARP. A failure to sense a P-wave, in turn, causes an atrial stimulus to be generated by the pacemaker that is more than likely delivered into the heart's atrial refractory period, at a time when such pulse is ineffective. This results in an effective prolongation of the P-to-V interval, which may either decrease hemodynamic performance and/or induce retrograde conduction. Even worse, the possibility exists that the atrial stimulus (delivered into the heart during the atrial refractory period) may induce atrial flutter or fibrillation. It is thus apparent that what is needed is a dual-chamber pacemaker that enhances its upper rate behavior so as to assure that any atrial stimulus will be effective, thereby minimizing the risk of retrograde conduction and induction of a PMT or atrial arrhythmias. There is also a need, in enhancing the upper rate response, to assure that pathological atrial rhythms are not tracked, thereby providing a more appropriate ventricular rate.
Several approaches are known in the art to minimize the likelihood of a PMT in patients having a dual-chamber pacing system. For example, for patients who are particularly prone to atrial arrhythmias and where tracking of fast atrial rates is not desirable, the pacing system can simply be programmed to operate in a DDI mode. The DDI mode operates the same as the DDD mode except that the atrial signals (P-waves) are not tracked. Hence, detection of P-waves in the DDI mode results in inhibition of atrial output, with normal ventricular timing. Thus, reversion to DDI pacing has proven to be an effective technique for minimizing the likelihood of PMT's for such patients.
Unfortunately, when pacing in the DDI mode, a sensed P-wave may result due to retrograde conduction, and therefore occur at a time in the cardiac cycle that is not hemodynamically efficient, i.e., at a time that is not appropriately synchronized with the next scheduled ventricular stimulation. That is, a hemodynamically efficient P-wave is one that occurs at a time in the cardiac cycle that provides "atrial kick" to fill the ventricles with blood just prior to the delivery of the next ventricular stimulation pulse pursuant to the pacemaker-determined ventricular timing (which is not altered by a sensed retrograde P-wave). It would be desirable, therefore, to provide a modified DDI response that improves the hemodynamic performance of the patient's heart, providing the needed "atrial kick" when appropriate, and not providing it when not appropriate.